Published January 1, 2019
| Version v1
Journal article
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Genetic Deficiency and Biochemical Inhibition of ITK Affect Human Th17, Treg, and Innate Lymphoid Cells
Creators
- 1. Erciyes Univ, Genome & Stem Cell Ctr GENKOK, Dept Med Biol, Fac Med, TR-38030 Kayseri, Turkey
- 2. Erciyes Univ, Div Pediat Hematol Oncol, Dept Pediat, Fac Med, TR-38030 Kayseri, Turkey
- 3. Ludwig Maximilians Univ Munchen, Univ Hosp, Dept Pediat, Dr von Hauner Childrens Hosp, Munich, Germany
Description
Purpose Interleukin-2-inducible T cell kinase (ITK) is an important mediator of T cell receptor signaling. Loss of function mutations in ITK results in hypogammaglobulinemia and CD4+ T cell loss in humans, and the patients often present with EBV-associated B cell lymphoproliferative syndrome. Itk-deficient mice show loss of T cell naivety, impaired cytolytic activity of CD8+ T cells, and defects in CD4+ T cell lineage choice decisions. In mice, Itk mutations were shown to affect Th17-Treg lineage choice in favor of the latter. In this study, we explored whether human ITK reciprocally regulates Th17-Treg balance as its murine ortholog.
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